parkinson's disease

symptoms

Parkinson’s is a neurodegenerative condition, meaning that cells in the brain are dying. What differentiates Parkinson’s disease from other neurodegenerative diseases is the area of the brain that is dominantly affected by the disease. While Alzheimer’s tends to affect the area of the brain over and behind the ears that control functions of memory, Parkinson’s affects a deep area called the substantia nigra that affects control of movement. The neurons in this area that help tone movement do so using the neurotransmitter dopamine. Loss of these dopamine producing cells results in the symptoms of slow movements, rigidity with movement, and tremor while at rest. As these symptoms relate to movement they are termed the motor symptoms of the disease.

Other non-motor symptoms are also a feature of Parkinson’s and one or more may precede the onset of motor symptoms. These may include:

As occurs in other neurodegenerative diseases such as Alzheimer’s the disease process can be seen in the brain well before symptoms become obvious. About 60% of the dopamine producing cells are lost before the symptoms begin to appear. Given this amount of neuron loss, a comprehensive treatment program is required to help with repair and improved function.

causes

As with other neurodegenerative diseases Parkinson’s appears to be caused by a collection of multiple factors. These involve genetic predispositions and environmental factors. Similar to Alzheimer’s disease which is associated with the build-up of a potentially toxic protein called beta amyloid, Parkinson’s is associated with the build-up of a toxic protein called alpha synuclein. This protein eventually aggregates into more complex proteins called Lewy bodies. There is evidence to suggest that these Lewy bodies kill the dopamine producing neurons in the brain but also conflicting evidence that they are just part of the neurons response to the disease process.

The genetic factors in Parkinson’s disease are present in only 15% of patients. These patients typically have a family history of the disease. Environmental factors are thought to be more involved in the origin of Parkinson’s. There are two areas where a relationship has been established, toxicity from chemicals such as pesticides or heavy metal toxicity, and toxicity caused by microbes such as viruses or bacteria.

Pesticides are strongly associated with Parkinson’s disease risk. A standard research model to induce Parkinson’s disease activity in laboratory animals is to give them the pesticide rotenone. Rotenone has been used as a broad-spectrum insecticide used as a topical powder to treat lice in humans and to treat parasitic mites in livestock and pets.

Higher rates of Parkinson’s disease have been demonstrated in several studies of workers using insecticides, herbicides and fungicides. Once this relationship was known, studies were extended to look at exposure and the disease not related to occupational exposure.

Studies looking at disease rates in different residential settings based on proximity to perhaps the highest use of these chemicals, agriculture, have demonstrated a relationship. Those living closer to commercial agricultural areas have higher rates of the disease. This relationship is dose dependent meaning the closer one lives to agriculture the greater the risk. Exposure is thought to occur both through air and ground water use.

An unexplored area is the relationship to herbicide contamination in food. The volume of the most commonly used herbicide, glyphosate, has increased from 3.5 billion pounds annually in the US in 1974 to a staggering 53 billion pounds per year currently. This explosive growth is driven by genetically modified crops, modified to tolerate glyphosate spraying for weed control. Trace residuals are found in food made from these crops as well as in ground water.

Other chemicals such as PCBs are associated with Parkinson’s risk. They are currently banned in the US because of their disease association, but significant amounts still remain in our environment and exposure occurs through fish, animal and plant consumption.

Heavy metal and transition metal toxicity is also related to Parkinson’s risk. These may include mercury, cadmium, arsenic, copper and perhaps excessive iron.

The primary cellular event causing Parkinson’s disease is loss of mitochondrial function. Mitochondrial are the energy producing bodies within cells. When these bodies are functioning well, they take in intermediates made from dietary energy sources such as sugars, fatty acids and amino acids and convert them into the final usable form of energy, ATP.

In this process of cell energy production, some molecules are incompletely broken down creating injurious products called free radicals. When most energy is properly broken down into ATP only a small amount of free radicals are produced, and the available antioxidants are able to inactivate them preventing cell injury. When the steps in producing ATP are impaired, excessive free radicals are produced eventually causing cell death.

Toxins have been found to interfere with this process of energy production causing excessive injurious free radical production and cell death. The final steps in ATP production involve processing energy intermediates across a series of enzymes called cytochromes. The pesticide rotenone blocks the first enzyme, complex I or cytochrome I. Other toxins block the third enzyme, complex III or cytochrome C.

Several steps in treatment can be used to restore cell energy production and minimize injurious free radical production. The first is to identify toxicity using a broad group of lab tests. Once that is done, attention to the source of exposure is important.

The next step is a targeted program of detoxification. This involves a program of herbs and nutrients that help cells and then the body effectively eliminate toxins. It also involves activating the body’s own cellular detoxifiers such as glutathione. Ironically in Parkinson’s disease the difficulty cells have with energy production impairs their ability to produce glutathione reducing detoxification capability. Different forms of glutathione are used until cells regain the ability to produce adequate amounts.

Once the prior two steps address toxicity, mitochondrial and cell repair is necessary to restore function. This step involves several targeted nutrients that the cell energy producing enzymes use to activate. A key step in the final mitochondrial process to produce ATP is increasing the activity of the third enzyme in the chain, cytochrome C. This is a photosensitive enzyme meaning that it can be activated by light, a process called photobiomodulation (link to PBM under services). Specific forms of “light” are needed to penetrate the skull to the areas involved in the disease. Pulsed or “cold” laser or infrared light can be used for this.

toxic exposure & neurodegeneration

The process of treating Parkinson’s disease is a complex and gradual process. The first step is to isolate sources of toxicity which may be driving the process. Once that is underway, efforts turn to detoxification and brain rehabilitation. Fortunately, we are learning more about how to do this effectively.